Neurapraxia is a temporary loss of function without discontinuity of the axon. The mildest form arises from the injection of a local anesthetic or a transient loss of circulation, such as with leg crossing. The changes are reversible. The reversibility can occur within a few weeks to a few months. Conduction velocity may be reduced, and focal demyelination may occur. In demyelinating neuropathies, associated neurapraxia is a major cause of paralysis.

Axonotmesis is a loss of continuity of the axons and their myelin sheaths, with preservation of the connective tissue. It usually occurs 4 or 5 days after an acute disruption. The distal segment becomes inexcitable as a result of nerve fiber degeneration (Wallerian degeneration). A complete conduction block may occur, such as in neurapraxia. Conduction velocity may remain normal in partial axonotmesis, as the intact axons conduct normally. In a motor nerve, the compound muscle action potential would be reduced in amplitude in proportion to the amount of axonal loss. Electromyography would show evidence of axonal loss in the form of fibrillation potentials and sharp positive waves 2–3 weeks after the occurrence of axonotmesis. Axons regenerate at a rate of approximately 1–3 mm per day.